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. 2020 Nov;37(11):4568-4584.
doi: 10.1007/s12325-020-01483-y. Epub 2020 Sep 5.

Relation of High Lipoprotein (a) Concentrations to Platelet Reactivity in Individuals with and Without Coronary Artery Disease

Rocío Salsoso  1 , Talia F Dalcoquio  1 , Remo H M Furtado  1   2 , André Franci  1 , Carlos J D G Barbosa  1   3 , Paulo R R Genestreti  1 , Celia M C Strunz  1 , Viviane Lima  1 , Luciano M Baracioli  1 , Robert P Giugliano  4 , Shaun G Goodman  5 , Paul A Gurbel  6 , Raul C Maranhão  7   8 , Jose C Nicolau  9
Affiliations

Relation of High Lipoprotein (a) Concentrations to Platelet Reactivity in Individuals with and Without Coronary Artery Disease

Rocío Salsoso et al. Adv Ther. 2020 Nov.

Abstract

Introduction: Lipoprotein (a) [Lp(a)] is a risk factor for coronary artery disease (CAD). To the best of our knowledge, this is the first study addressing the relationship between Lp(a) and platelet reactivity in primary and secondary prevention.

Methods: Lp(a) was evaluated in 396 individuals with (82.3%) and without (17.7%) obstructive CAD. The population was divided into two groups according to Lp(a) concentrations with a cutoff value of 50 mg/dL. The primary objective was to evaluate the association between Lp(a) and adenosine diphosphate (ADP)-induced platelet reactivity using the VerifyNow™ P2Y12 assay. Platelet reactivity was also induced by arachidonic acid and collagen-epinephrine (C-EPI) and assessed by Multiplate™, platelet function analyzer™ 100 (PFA-100), and light transmission aggregometry (LTA) assays. Secondary objectives included the assessment of the primary endpoint in individuals with or without CAD.

Results: Overall, 294 (74.2%) individuals had Lp(a) < 50 mg/dL [median (IQR) 13.2 (5.8-27.9) mg/dL] and 102 (25.8%) had Lp(a) ≥ 50 mg/dL [82.5 (67.6-114.5) mg/dL], P < 0.001. Univariate analysis in the entire population revealed no differences in ADP-induced platelet reactivity between individuals with Lp(a) ≥ 50 mg/dL (249.4 ± 43.8 PRU) versus Lp(a) < 50 mg/dL (243.1 ± 52.2 PRU), P = 0.277. Similar findings were present in individuals with (P = 0.228) and without (P = 0.669) CAD, and regardless of the agonist used or method of analysis (all P > 0.05). Finally, multivariable analysis did not show a significant association between ADP-induced platelet reactivity and Lp(a) ≥ 50 mg/dL [adjusted OR = 1.00 [(95% CI 0.99-1.01), P = 0.590].

Conclusion: In individuals with or without CAD, Lp(a) ≥ 50 mg/dL was not associated with higher platelet reactivity.

Keywords: Coronary artery disease; Lipoprotein (a); Platelet reactivity; Primary prevention.

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Figures

Fig. 1
Fig. 1
Distribution of lipoprotein (a) concentrations. Serum Lp(a) concentrations in mg/dL from 326 (82.3%) individuals with CAD and 70 (17.7%) individuals without CAD are shown in a frequency distribution histogram. Distribution are from Kolmogorov–Smirnov test (see “Methods”). Median (IQR) = 22.0 (7.9–52.2) mg/dL. Lp(a) lipoprotein (a), CAD coronary artery disease, IQR interquartile range
Fig. 2
Fig. 2
Association of ADP-induced platelet reactivity according to lipoprotein (a) concentrations in individuals stratified by the presence or absence of CAD. Univariate analysis was applied to determine the association between Lp(a) concentrations < 50 mg/dL and Lp ≥ 50 mg/dL versus ADP-induced platelet reactivity measured by VerifyNow™ P2Y12 (PRU) in a total of 396 individuals (a) which included 326 with CAD (b) and 70 without CAD (c). Values are median (IQR). P value are from Mann–Whitney test (see “Methods”). ADP adenosine diphosphate, CAD coronary artery disease, Lp(a) lipoprotein (a), PRU P2Y12 reaction units, IQR interquartile range
Fig. 3
Fig. 3
Association between lipoprotein (a) concentrations and ADP-induced platelet reactivity. Linear regression was represented for Lp(a) measured in mg/dL versus ADP-induced platelet reactivity evaluated by VerifyNow™ P2Y12 assay (PRU). Lp(a) lipoprotein (a), ADP adenosine diphosphate, PRU P2Y12 reaction units
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